Publications by authors named "Juliana Austin"

15 Publications

  • Page 1 of 1

Meeting Report: 2018 Annual Meeting of the Pediatric Endocrine Society, Toronto, Canada, May 5-8, 2018, Selected Highlights.

Pediatr Endocrinol Rev 2018 Dec;16(2):284-293

Children's Hospital Los Angeles, 4650 Sunset Blvd, MS #61, Los Angeles, CA 90027, USA, E-mail:

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http://dx.doi.org/10.17458/per.vol16.2018.lama.mr.pestorontoDOI Listing
December 2018

A germline mutation of HRPT2/CDC73 (70 G>T) in an adolescent female with parathyroid carcinoma: first case report and a review of the literature.

J Pediatr Endocrinol Metab 2016 Sep;29(9):1005-12

Parathyroid carcinoma is a rare cause of primary hyperparathyroidism amongst children, with only nine previously reported cases. The objective of the study was to present the first pediatric case with a germline CDC73 (formerly known as HRPT2) mutation, and to review the literature. A 14-year-old girl presented with pathologic slipped capital femoral epiphysis (SCFE). The patient was noted to have an elevated calcium level of 3.4 mmol/L (13.4 mg/dL), a parathyroid hormone (PTH) level of 1013 ng/L (1013 pg/mL), and a 3-cm palpable neck mass. Ultrasound and 99mTc-Sestamibi confirmed the suspicion of a parathyroid mass. Intraoperative findings and pathology confirmed the diagnosis of parathyroid carcinoma. Post-operative PTH decreased to 14 ng/L (14 pg/mL). Genetic testing showed a germline 70 G>T HRPT2/CDC73 mutation. This is the first case documenting a germline 70 G>T HRPT2/CDC73 gene mutation in a pediatric parathyroid carcinoma. Patients with sporadic parathyroid carcinoma may benefit from HRPT2/CDC73 gene mutation screening.
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http://dx.doi.org/10.1515/jpem-2016-0109DOI Listing
September 2016

Bone health in children and adolescents: risk factors for low bone density.

Pediatr Endocrinol Rev 2013 Mar-Apr;10(3):318-35

Center for Endocrinology, Diabetes, and Metabolism, Children's Hospital Los Angeles, Keck School of Medicine of USC, Los Angeles, CA 90027 USA.

Osteoporosis is a common disease that is characterized by low bone mineral density (BMD). Decreased BMD is associated with increased fracture risk. In adults, normal BMD results from the balance between accrual of peak bone mass (PBM) at the end of adolescence, and subsequent bone loss with age. Although environmental factors play a role, hereditary factors are the major contributors (up to 80%) to the variability in PBM. This review examines the effects of genetics, physical activity and immobilization, smoking, chronic diseases and medications, vitamin D, calcium, and various other dietary factors on bone integrity in children, adolescents, and adults.
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June 2013

2012 annual meeting of the Endocrine Society, Houston, Texas (June 23-26 2012) selected highlights.

Pediatr Endocrinol Rev 2012 Dec-2013 Jan;10(2):246-59

University of California, San Francisco, San Francisco, CA 94143-0434, USA.

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May 2013

Meeting highlights: Lawson Wilkins Pediatric Endocrine Society (PES) annual meeting, Denver Colorado, USA.

Authors:
Juliana Austin

Pediatr Endocrinol Rev 2011 Sep;9(1):481-5

Department of Pediatrics, Division of Pediatric Endocrinology, Long Beach Memorial and Miller Children's Hospital, Long Beach, CA, USA.

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September 2011

Disorders of sex development-when and how to tell the patient.

Pediatr Endocrinol Rev 2011 Mar;8(3):213-7; quiz 223

Department of Pediatrics, Division of Pediatric Endocrinology, Long Beach Memorial and Miller Children's Hospital, Long Beach, CA.

Physicians and other providers are often confronted with difficult decisions in the area of disclosure. This article examines a hypothetical situation relevant to the practice of pediatric endocrinology. The parents of a child with a disorder of sex development (DSD) wish the physician to treat their child, but without revealing key medical information to the child. Herein, we will explore the legal and ethical responsibilities of a provider to disclose information to an under-age DSD patient and to provide insight on when and how to tell the patient.
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March 2011

Meeting highlights: Endocrine Society, San Diego, California, June 19-22, 2010.

Pediatr Endocrinol Rev 2010 Dec;8(2):114-22

Children's Hospital Los Angeles, Los Angeles, CA 90027, USA.

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December 2010

2009 Annual Meeting of the Endocrine Society Washington DC, United States (June 10-13, 2009)--selected highlights.

Pediatr Endocrinol Rev 2009 Dec;7(2):50-8

Rady Children's Hospital, University of California, San Diego School of Medicine, San Diego, CA, USA.

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December 2009

Hormonal regulators of appetite.

Int J Pediatr Endocrinol 2009 3;2009:141753. Epub 2008 Dec 3.

Department of Pediatrics, Division of Endocrinology, Oregon Health & Science University, Portland, OR 97239, USA.

Obesity is a significant cause of morbidity and mortality worldwide. There has been a significant worsening of the obesity epidemic mainly due to alterations in dietary intake and energy expenditure. Alternatively, cachexia, or pathologic weight loss, is a significant problem for individuals with chronic disease. Despite their obvious differences, both processes involve hormones that regulate appetite. These hormones act on specific centers in the brain that affect the sensations of hunger and satiety. Mutations in these hormones or their receptors can cause substantial pathology leading to obesity or anorexia. Identification of individuals with specific genetic mutations may ultimately lead to more appropriate therapies targeted at the underlying disease process. Thus far, these hormones have mainly been studied in adults and animal models. This article is aimed at reviewing the hormones involved in hunger and satiety, with a focus on pediatrics.
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http://dx.doi.org/10.1155/2009/141753DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777281PMC
July 2011

How should we be treating children with congenital hypothyroidism?

J Pediatr Endocrinol Metab 2007 May;20(5):559-78

Department of Pediatrics, Division of Endocrinology, Oregon Health & Science University, Portland, OR 97239, USA.

Early detection by newborn screening and appropriate L-thyroxine treatment leads to normal or near-normal neurocognitive outcome in infants with congenital hypothyroidism. Many newborns with congenital hypothyroidism have some residual thyroid hormone production, and even in those with athyreosis, transplacental passage of maternal thyroid hormone offers some protection for a time. Given the serum T4 half-life of 6 days, the neonatal T4 level will fall and disappear over the first 2-3 weeks of life. Thus, there is a crucial 'window of opportunity' to correct the hypothyroidism and minimize the time the brain is exposed to hypothyroxinemia. While there are few truly prospective, randomized clinical trials investigating treatment parameters, studies measuring IQ outcome support a starting L-thyroxine dose of 10-15 microg/kg/day. Further, studies show that the most severely hypothyroid infants are at risk for a 5-20 point decrease in IQ. Such infants may benefit from a starting dose of 12-17 microg/kg/d, which has been shown to normalize T4 in 3 days and TSH in 2 weeks. Target serum T4 or free T4 levels appear to be higher in the first two weeks of treatment. Infants require more frequent laboratory monitoring, every 1-2 months in the first 6 months and every 3-4 months until age 3 years, as the developing brain has a critical dependence on thyroid hormone in the first 2-3 years of life.
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http://dx.doi.org/10.1515/jpem.2007.20.5.559DOI Listing
May 2007

Salt-wasting 21-hydroxylase deficiency congenital adrenal hyperplasia and pyloric stenosis in two Hispanic brothers.

J Pediatr 2006 Aug;149(2):268-70

Center for Endocrinology, Diabetes and Metabolism, Childrens Hospital Los Angeles, Department of Pediatrics, University of Southern California, Keck School of Medicine, Los Angeles, California 90027, USA.

The differential diagnosis of vomiting and dehydration in the first month of life includes congenital adrenal hyperplasia (CAH) and pyloric stenosis (PS). Each diagnosis may mask the presence of the other, requiring careful evaluation and follow-up. We document the occurrence of CAH and PS in two Hispanic siblings.
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http://dx.doi.org/10.1016/j.jpeds.2006.03.007DOI Listing
August 2006

Characteristics of glycemic control in young children with type 1 diabetes.

Pediatr Diabetes 2002 Dec;3(4):179-83

Department of Pediatrics, Children's Hospital Los Angeles and USC School of Medicine, Los Angeles, CA 90027, USA.

Background: The Diabetes Control and Complications Trial (DCCT) demonstrated that the rate-limiting step to the intensification of diabetes management in adolescents and adults was hypoglycemia. Young children were presumed to be at even greater risk for hypoglycemia with severe consequences, particularly if they had HbA1c levels < 8%.

Subjects: A retrospective chart review was performed on 148 patients with type 1 diabetes on insulin injection therapy who were < 8 yr of age (mean age 5.7 +/- 1.5, mean diabetes duration 3.0 +/- 1.4 yr) followed quarterly from July 1999 to June 2001.

Methods: The subjects were divided into two groups based on their mean HbA1c values (< 8 vs. > or = 8%) averaged over the 2-yr time period. The following variables were analyzed comparing the two groups: age, duration of diabetes, insulin dose, severe hypoglycemic episodes, episodes of diabetic ketoacidosis (DKA), percentage of glucose levels above, within, and below the target range, and number of diabetes home-management competencies obtained.

Results: Patients with HbA1c < 8% spent more time within target range (40.0 vs. 29.5%, p = 0.0001) and less time above their target range (36.9 vs. 51.2%, p = 0.0003). There was no difference in the percentage of glucose levels below target (23.2 vs. 19.4%, p = NS), percentage of severe hypoglycemic episodes (3 vs. 7 episodes per 100 patient-yr, p = NS), or episodes of DKA (1 vs. 3 episodes per 100 patient-yr, p = NS) between the two groups. SUBJECTS with lower HbA1c levels had acquired more home-management competencies (4.0 vs. 3.5, p = 0.01).

Conclusions: If families are competent in fundamental diabetes management, young children can achieve HbA1c levels < 8.0% without increasing the risk of hypoglycemia.
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http://dx.doi.org/10.1034/j.1399-5448.2002.30402.xDOI Listing
December 2002

Nocturnal hypoglycemia detected with the Continuous Glucose Monitoring System in pediatric patients with type 1 diabetes.

J Pediatr 2002 Nov;141(5):625-30

Department of Pediatrics, University of Southern California School of Medicine, Los Angeles, California, USA.

Objective: To use the Continuous Glucose Monitoring System (CGMS, MiniMed, Sylmar, Calif) to determine if bedtime blood glucose levels were associated with the occurrence of nocturnal hypoglycemia.

Study Design: Patients (n = 47, 18 boys, mean age 11.8 +/- 4.6 years) with type 1 diabetes used CGMS for 167 nights. Data were analyzed for glucose 100 mg/dL and 150 mg/dL.

Results: A glucose value of 100 mg/dL, P = NS), and no bedtime glucose value between 110 and 300 mg/dL decreased the incidence of nocturnal hypoglycemia to
Conclusions: Nocturnal hypoglycemia is frequent, of long duration, associated with bedtime glucose values
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http://dx.doi.org/10.1067/mpd.2002.129175DOI Listing
November 2002
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